TY  - JOUR
A1  - Relja, Borna
A1  - Omid, Nina
A1  - Kontradowitz, Kerstin
A1  - Jurida, Katrin
A1  - Oppermann, Elsie
A1  - Störmann, Philipp
A1  - Werner, Isabella
A1  - Jüngel, Eva
A1  - Seebach, Caroline
A1  - Marzi, Ingo
T1  - Decreased inflammatory responses of human lung epithelial cells after ethanol exposure are mimicked by ethyl pyruvate
T2  - Mediators of inflammation
N2  - Background and Purpose. Leukocyte migration into alveolar space plays a critical role in pulmonary inflammation resulting in lung injury. Acute ethanol (EtOH) exposure exerts anti-inflammatory effects. The clinical use of EtOH is critical due to its side effects. Here, we compared effects of EtOH and ethyl pyruvate (EtP) on neutrophil adhesion and activation of cultured alveolar epithelial cells (A549). Experimental Approach. Time course and dose-dependent release of interleukin- (IL-) 6 and IL-8 from A549 were measured after pretreatment of A549 with EtP (2.5–10 mM), sodium pyruvate (NaP, 10 mM), or EtOH (85–170 mM), and subsequent lipopolysaccharide or IL-1beta stimulation. Neutrophil adhesion to pretreated and stimulated A549 monolayers and CD54 surface expression were determined. Key Results. Treating A549 with EtOH or EtP reduced substantially the cytokine-induced release of IL-8 and IL-6. EtOH and EtP (but not NaP) reduced the adhesion of neutrophils to monolayers in a dose- and time-dependent fashion. CD54 expression on A549 decreased after EtOH or EtP treatment before IL-1beta stimulation. Conclusions and Implications. EtP reduces secretory and adhesive potential of lung epithelial cells under inflammatory conditions. These findings suggest EtP as a potential treatment alternative that mimics the anti-inflammatory effects of EtOH in early inflammatory response in lungs.
Y1  - 2014
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/41957
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-419577
N1  - Copyright © 2014 B. Relja et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
VL  - 2014
IS  - Article ID 781519
SP  - 1
EP  - 13
ER  -